tbuckley/cabot-search huggingface dataset:
Abstract 9492: Transcatheter Amplatzer Occluder Device Closure of Post-Myocardial Infarct Pseudoaneurysm: A Case Report
Authors: Yaswanraj Yuvaraj, Michael Girard, Marquand B Patton
Journal: Circulation (2022)

Introduction: Left Ventricular Pseudoaneurysm (LVP) is defined as cardiac wall rupture leading to a formation of wall with thrombus, pericardial, or scar tissue functioning as a pouch for blood. A loculated pericardial effusion (LPE), and right ventricular pericardial fistula (RVPF) have never been reported in literature. Here, we report the first case of a 70 year old male who developed a LVP, LPE, and RVPF. Case Description: A 70 year old male with a past medical history of hypertension presented with inferior wall STEMI. Cardiac catheterization demonstrated left anterior descending (LAD) with 80% occlusion and right coronary artery (RCA) with 100% occlusion. Percutaneous intervention of RCA with aspiration thrombectomy and two drug eluting stents was performed. Echocardiogram the following day demonstrated a LVP. A transesophageal echocardiogram (TEE) demonstrated LVP near the mid-inferior interventricular septum draining into the pericardial space, and LPE from the apical inferior left ventricle (LV) extending to the apical cap of the right ventricle (RV). Computed tomography angiography (CTA) demonstrated a multiloculated collection at the inferior septal aspect of LV contained by the pericardial space. Patient was a high risk for surgery. LVP was closed via a 24 mm atrial septal defect (ASD) occluder device. Intraoperative TEE demonstrated an ASD occluder device at the mid inferior septum at the location of the LVP neck with minimal residual flow into the LPE and a fistula connecting the LPE space with RV. RVFP was managed conservatively. LAD was managed medically. Patient was discharged home safely on guideline directed medical therapy. Discussion: LVP rate is 0.0026% following myocardial injury. It is reported that untreated LVP have a rupture risk of about 30% and a mortality rate of 50%. Prompt treatment is required to prevent mortality. Surgical management is the standard of care. A multidisciplinary heart team deemed the patient a high risk. Therefore, transcatheter treatment was sought in the patient above. Conclusions: Surgical treatment is standard of care for LVP, but transcatheter wall closure with an ASD device is a promising technique not only for high-risk surgical candidates such as above, but as a gold standard of treatment for LVP.
Abstract 9538: Impact of Device Closure on Heart Failure Progression in Patients With Patent Foramen Ovale
Authors: Jiesuck Park, Hong-Mi Choi, In-chang Hwang, Yeonyee E Yoon, Jae Hyeong Park, Goo-Yeong Cho
Journal: Circulation (2022)

Background: Patent foramen ovale (PFO) can unload left atrial pressure via interatrial shunt. We evaluated whether device occlusion of PFO is associated with subsequent risk of heart failure (HF). Methods: We enrolled 4,804 consecutive patients (median age: 68 years, 62.4% male) who underwent transesophageal echocardiography at tertiary medical centers in Korea between 2007 and 2019. The primary outcome was the 4-year risk of HF. The independent association of PFO closure with HF was evaluated using the Cox regression hazard model after multivariate adjustment for demographics, clinical risk factors, and echocardiographic parameters. Additional subgroup analysis was performed according to the presence structural heart disease defined as left ventricular (LV) ejection fraction &lt; 55%, left atrial (LA) size &gt; 35ml or LA volume ≥ 40ml/m 2 , LV mass index ≥ 115g/m 2 , E/e' ≥ 15, or presence of atrial fibrillation. Results: In total, PFO was observed in 981 (20.4%) patients, where 161 (16.4%) of them underwent device closure. Patients with PFO showed a lower risk of HF than those without (2.6 vs. 4.0%, adjusted hazard ratio [HR]: 0.65, 95% confidence interval [CI] 0.45-0.94, p=0.021). PFO closure group showed a significantly higher risk of HF than no closure group (5.5 vs. 1.2%, adjusted HR: 5.59, 95% CI 4.26-7.34, p&lt;0.001) (Figure). In subgroup analysis, PFO closure was significantly associated with HF risk in patients with underlying structural heart disease (9.6 vs. 3.9%, adjusted HR: 2.55, 95% CI 1.95-3.33, p&lt;0.001), demonstrating an increasing trend in proportion to the number of structural abnormalities. However, PFO closure showed no significant association with HF risk in patients without structural heart disease (1.7 vs. 1.5%, adjusted HR: 1.22, 95% CI 0.99-1.50, p=0.054). Conclusion: PFO closure may increase the risk of HF. Therefore, careful patient selection is needed, especially among those with underlying structural heart disease.
Abstract 9271: Risk of Cancer After Diagnosis of Cardiovascular Disease
Authors: Caitlin Bell, Xiudong Lei, Richard Baylis, Hua Gao, Lingfeng Luo, Sharon Giordano, Mackenzie Wehner, Kevin Nead, Nick J Leeper
Journal: Circulation (2022)

Introduction: Cardiovascular disease (CVD) and cancer share several known risk factors. While preclinical models have found that various types of CVD can accelerate cancer progression, clinical studies have not determined whether these associations are due to shared risk factors or a specific impact of atherosclerosis on cancer development. Hypothesis: CVD, particularly atherosclerotic CVD, is an independent risk factor for incident cancer. Methods: We used a 1:1 matched retrospective cohort study using IBM’s MarketScan insurance claims database from 2009 to 2019. Those with CVD were stratified as having either atherosclerotic (aCVD) or non-atherosclerotic disease (naCVD). Those with prior diagnostic codes for cancer were excluded. Cumulative risks of (1) any incident cancer, (2) organ-specific cancers according to CVD groups. Kaplan-Meier and multivariable adjusted Cox proportional hazards (PH) models with propensity score adjustment were used to evaluate the association of CVD groups and cancer. Results: Among 4,487,412 matched (1:1 no CVD vs. CVD) individuals, the mean age was 56 years, 48% were female, 31% had aCVD, and 19% had naCVD. Those without CVD had a 5-year cumulative cancer incidence of 5.4% (95% CI, 5.3%-5.4%), compared to 6.8% (95% CI, 6.7%-6.8%) among those with any CVD and 7.7% (95% CI, 7.6%-7.8%) for those with aCVD. After multivariable and propensity score adjustment, individuals with CVD were found to have a significantly increased risk of incident cancer compared to individuals without CVD (hazard ratio [HR], 1.14; 95% CI, 1.13-1.15). Those with aCVD had a significantly higher risk of cancer compared to the naCVD group (HR, 1.03; 95% CI, 1.02-1.05). These findings were consistent in sensitivity analyses which were further adjusted for smoking history and body mass index. Cancer subtype analyses showed a specific association of aCVD with lung, bladder, liver, brain, and other hematologic cancers. Conclusions: In this retrospective cohort study, individuals with CVD had an increased risk of incident cancer compared to those without CVD. This association may be driven by the relationship of aCVD with specific cancer subtypes, which persists after controlling for conventional risk factors.
Abstract 9407: Long-Term Outcomes of Hospitalized Acute Myocarditis: A Korean Nationwide Data in the Pre-COVID-19 Era
Authors: Mi-jeong Kim, Hae-Ok Jung, Hoseob Kim, Yoonjong Bae, Doo-Soo Jeon, Kyung Ahn Kim, Soyoung Lee, Soohyun Kim, Soyoon Park
Journal: Circulation (2022)

Introduction: Acute myocarditis is extremely heterogenous in causal agents, clinical courses, and geographic regions. There is little long-term outcomes data for acute myocarditis prior to the COVID-19 pandemic. Hypothesis: The clinical profile of acute myocarditis would differ according to age at presentation. Methods: A retrospective nationwide cohort study was performed. All patients aged 20-79 who were hospitalized for acute myocarditis without underlying cardiac diseases from 2006 to 2018 in Korea. Complicated phenotype was defined as requiring hemodynamic or major organ support. Over 10 years, all-cause mortality and acute myocarditis-driven excess mortality were evaluated according to young-adult (20-39 years), mid-life (40-59 years), and older-adult (60-79 years) age groups. Results: Among 2988 patients (mean age 51.0 years), 362 (12.1%) were of complicated phenotype. All-cause death at 30 days occurred in 40 (4.7%), 52 (4.8%), and 105 (10.0%) patients in the young-adult, mid-life, and older adult groups, respectively (Figure A). Most short-term deaths occurred within 37 days of admission, primarily in the complicated phenotype. However, higher excess mortality compared to the age- and sex-matched general population remained over the 10-year follow-up even in younger patients with non-complicated phenotypes (Figure B). Conclusions: In patients with de novo acute hospitalized myocarditis, short-term mortality is high both in young and older adults, particularly those with advanced age, non-cardiac comorbidities, and severe clinical presentation. Furthermore, long-term excess mortality remains high over 10 years after index hospitalization. A cardiac monitoring strategy should be discussed for post-myocarditis patients against the long-term risk.
Abstract 9548: Dual Energy Computed Tomography Perfusion Mapping of Coronary to Pulmonary Collaterals in Chronic Thromboembolic Pulmonary Hypertension
Authors: Ansh Goyal, Michael Cuttica, James D Flaherty, Christopher C Malaisrie, Ruben Mylvaganam
Journal: Circulation (2022)

Introduction: Chronic thromboembolic pulmonary hypertension (CTEPH) is classified as group 4 pulmonary hypertension where unresolved thromboembolic disease obstructs the pulmonary artery. The resultant lung ischemia commonly leads to bronchopulmonary collateralization thought to lower pulmonary vascular resistance and reduce mortality. Here, we present a rare presentation of coronary-pulmonary collaterals in a 65-year-old former 40-pack year smoker with CTEPH, COPD requiring oxygen, AF, and DHF. Results: Dual-energy computed tomography (DECT) showed complete occlusion of the proximal right pulmonary artery. However, perfused blood volume (PBV) mapping of the DECT study revealed areas of the right lung that were still minimally perfused (Figure 1A, B). Pulmonary angiography confirmed occlusion of the right pulmonary artery (1C) . Subsequent coronary angiography revealed the presence of coronary to pulmonary collaterals that were providing limited perfusion to the right pulmonary circulation from the left circumflex artery (1D) . The patient underwent pulmonary thromboendarterectomy with removal of the clot en bloc without complication (1E) . Post-surgery DECT confirmed restoration of pulmonary arterial circulation and catheterization revealed an excellent hemodynamic response to surgery (1F, G) . Conclusions: DECT-derived PBV revealed significant perfusion to a proximally obstructed lung, hastening the discovery of rarely documented coronary-pulmonary artery collaterals via coronary angiography. We uniquely visualize via perfusion mapping that the collaterals provide an alternate vascular supply distal to the chronic pulmonary arterial obstruction until thromboendarterectomy can conclusively treat the occlusion. The presence of coronary-pulmonary collaterals may share similar pathophysiology to bronchial-pulmonary collaterals and be a positive prognosticator for robust post-operative hemodynamic improvement in CTEPH.
Abstract 9419: Empagliflozin Modulates Cardiac Na Homeostasis via Late I <sub>Na</sub> and I <sub>NCX</sub>
Authors: Julian Mustroph, Maria Baier, Maximilian Trum, Steffen Pabel, Thea Stehle, Zdenek Provaznik, Samuel Sossalla, Lars S Maier, Stefan Wagner
Journal: Circulation (2022)

Introduction: The effects of empagliflozin on excitation-contraction coupling (ECC) have not been fully elucidated. We previously showed that empagliflozin directly reduces Ca 2+ /calmodulin kinase II (CaMKII) activity in human and murine heart failure, thereby improving contraction. Upon acute exposure, however, only subsarcolemmal [Na + ] is decreased, while [Na + ] cytosolic and [Ca 2+ ] cytosolic are only decreased after 24 h empagliflozin. Hypothesis: We hypothesize that empagliflozin reduces cardiac late Na current (late I Na ) via a reduction in CaMKII activity. We further hypothesize that Na + /Ca 2+ -exchanger (NCX) is acutely masking effects on cardiac [Na + ], thereby delaying downstream effects on cardiac ECC. Methods: Informed consent was obtained according to the Declaration of Helsinki. Human/murine cardiomyocytes (CM) were isolated and incubated with 1 μM empagliflozin for 30 min or 24 h. Some CM were treated with H 2 O 2 or ATX-II to induce late I Na . Whole-cell patch clamp was used to measure late I Na or I NCX . Epifluorescence with SBFI was used to obtain cardiac [Na + ]. Some CM were treated with NCX inhibitor KB-R7943 (5 μM). Results and Conclusions: Late I Na induced by H 2 O 2 was acutely inhibited in human and murine CM by empagliflozin, similar to CaMKII inhibition with AIP (2 μM). In CM lacking CaMKII or the CaMKII phosphosite S571 on Na V 1.5, no effect of empagliflozin on late I Na was present (also not under ATX-II stimulation). As shown before, subsarcolemmal [Na + ] estimated via patch clamp (Nernst equation) was already reduced after 30min (T30 min ). However, empagliflozin did not acutely reduce cytosolic [Na + ] at T30 min , but potently did so after 24h exposure (SBFI measurement). Acute inhibition of NCX with KB-R7943 showed no effect on cardiac Na + , but when performed in addition to empagliflozin, potently reduced [Na + ] already at T30 min . Matching this, NCX forward mode (patch clamp) was acutely induced by empagliflozin at T30 min , thus resulting in Na + influx that initially masks the reduction in [Na + ] resulting from a reduction in late I Na . This may explain why Na + /Ca 2+ homeostasis is only affected after 24h empagliflozin exposure. Our results may explain discrepant results on ECC by different groups on acute vs. prolonged empagliflozin exposure.
Abstract 9578: Chronic Phosphodiesterase Type 5 Inhibition by Sildenafil Causes Regression of Heart Failure: Insights into Molecular and Cellular Mechanisms
Authors: Tiankai Li, Heng-Jie Cheng, Xiaowei Zhang, Zhi Zhang, David X Zhao, David M Herrington, Dalane W Kitzman, Che Ping Cheng
Journal: Circulation (2022)

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). However, whether and by what mechanisms SIL can stop the progression of HF, or maybe even reverse the clinical route remain unknown. We tested the hypothesis that chronic SIL would improve intrinsic myocyte function and [Ca 2+ ] i regulation and reverse HF-induced detrimental alterations on cardiac SERCA2a, β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms, thus playing a salutary role in HF. Methods: We evaluated LV and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SR Ca 2+ -ATPase (SERCA2a), phospholamban (PLB), and 3 NOS in 3 groups of male rats (8/group) for a period of 3 months (M): 1) HF , 3 M after receiving isoproterenol (ISO) (170 mg/kg sq for 2 days); 2) HF/SIL , 2 M after ISO, then SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and 3) Controls . Results: Versus C, ISO-treated rats progressed to severe HF at 3 M with significantly reduced LV contractility (E ES , 0.7 vs 1.1 mmHg/μl), and slowed LV relaxation. LV myocyte contraction (dL/dt max , 77 vs 136 μm/sec), relaxation (dR/dt max , 62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) were significantly decreased accompanied by a diminished myocyte inotropic response to ISO (10 -8 M) superfusion. These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio, and eNOS (0.28 vs 0.46), but increased protein levels of β 3 -AR (0.23 vs 0.10) and iNOS (0.18 vs 0.08). Chronic SIL treatment prevented HF-caused reduced E ES (1.3 mmHg/μl) and EF (62%) and retained normal dL/dt max (131μm/s), dR/dt max (106 μm/s), and [Ca 2+ ] iT (0.24), and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were normalized to control values, but eNOS was significantly elevated (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverses contrast changes between iNOS and β 3 -AR with SERCA2a and eNOS expression, restores normal myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve, and leads to regression of LV dysfunction in a rat model of progressive HF.
Abstract 9442: Increasing Patient Activation Among Black American Men in a Community-Based Lifestyle Intervention Pilot: Black Impact
Authors: Sarah Addison, Amaris Williams, Jing Zhang, Faith Metlock, Yesol Yang, John Gregory, Darrell Gray, Timiya S Nolan, Joshua J Joseph
Journal: Circulation (2022)

Introduction: Life’s simple 7 (LS7) is a seven-metric framework from which cardiovascular health can be measured. Black Americans have the lowest attainment of LS7 among all communities. This may be in part related to patient activation or “having the capability and the willingness to take on the role of managing one’s own health and health care”. Patients with lower patient activation scores on the Patient Activation Measure tool (PAM) are more likely to develop and suffer from chronic diseases like hypertension and stroke. Black Americans report lower patient activation as compared to Non-Hispanic Whites, and lower medication adherence. Here, we discuss changes in patient activation during a 24-week community-based, lifestyle intervention focused on improving cardiovascular health in Black American men. Methods: We recruited 74 Black men with less than 4 of 7 LS7 metrics in the “ideal” range to participate in Black Impact, a community-based lifestyle intervention adapted from the AHA’s Check, Change, Control Program and Diabetes Prevention Program. Participants met weekly in groups of 8-25 for 24 weeks, completing group-based physical activities and health education sessions. Biometric screenings and self-report surveys (including the PAM 10-item questionnaire) were administered at baseline, 12, and 24 weeks. Changes in PAM scores at 12 and 24 weeks were calculated using a linear mixed-effects model with random intercepts. Results: The mean baseline PAM score of participants, when adjusted for age, education, and income, was 64.68 (95% CI: 60.51, 68.85). At week 12, the PAM score increased by an average of 4.36 (95% CI: 1.09, 7.63; p = 0.01). At week 24, the increase from baseline was 8.22 (95% CI: 5.06, 11.38; p &lt; 0.001). Increases in PAM were non-significantly associated with increases in LS7 over the 24 weeks (p= 0.346) Conclusions: In Black Impact, PAM scores increased substantially at 12 and 24 weeks. The 8-point PAM increase at 24 weeks is equivalent to a 16% reduction in the likelihood of hospitalizations and a 16% increase in medication adherence. These findings suggest community-based lifestyle interventions focused on increasing cardiovascular health may be a key strategy in advancing equity in patient activation.
Abstract 9616: A Cardiac Mass in the Postpartum: A Diagnostic and Therapeutic Dilemma
Authors: Elena Dudorova, Stefano Ravalli
Journal: Circulation (2022)

Introduction: Precise diagnosis of a cardiac mass has crucial prognostic and therapeutic implications. Case Presentation: A 23-year-old woman presented to an outside hospital 6 days after delivery with headaches, chest pain and very high BP. A CT angiogram found no pulmonary emboli but identified a mass in the right atrium. Surgical removal was attempted but had to be aborted because of inability to get clear margins. Frozen section showed atypical spindle cells, suggestive of sarcoma. Patient was transferred to our hospital for further management. TTE (Figure) revealed a large solid mass almost entirely filling the right atrium and a small pericardial effusion. CMR showed a 7.2 cm hypervascular mass in the right atrium with possible invasion of the superior vena cava, suggestive of angiosarcoma. Additional tissue sections showed vascular spaces lined by benign endothelial cells positive for the endothelial markers ERG, CD31 and CD34 and infiltrating the underlying myocardium; proliferation rate was &lt;1%. Based on these findings a diagnosis of primary cardiac hemangioma was made. Subsequent PET CT showed mildly FDG-avid cardiac mass and no metastases. Discussion: Cardiac masses are a diagnostic challenge. Identification hinges on clinical history, location and multimodality imaging but histopathology and immunohistochemistry remain the gold standard for a definitive diagnosis. Primary cardiac tumors are rare, found only in &lt;0.05% of autopsies; 80% are benign and 20% malignant. Hemangiomas are extremely rare, representing &lt;3% of primary cardiac tumors. They are often misdiagnosed as other neoplasms, as was the case in our patient, possibly leading to unnecessary invasive procedures. Although benign, hemangiomas can infiltrate surrounding structures and cause serious complications, such as syncope, emboli, arrhythmias, heart block and stroke. Complete surgical excision remains the treatment of choice and, if successful, confers a positive prognosis.
Abstract 9796: Identification of an Optimal Blood Pressure by Images of Correction of the Pathological Mechanism by Hypertension: An Angiographic, Machine Learning Analysis and Application for Personalized Medicine
Authors: Thach N Nguyen, Wei Hsu Che, Lan T Ly, Thoa Le, THIEN PHAM, Quang Phuc Vu, Nga Nguyen, DUC Nguyen, BAO Nguyen, Quang Dat Ha, Duong Huynh, Sarthak Aggarwal, Imran Mihas, LOC Vu, Cardy Nguyen
Journal: Circulation (2022)

Introduction: As hypertension (HTN) is a strong risk factor of coronary artery disease (CAD), what is an optimal blood pressure (BP) which could preclude CAD? Hypothesis: In industrial piping, laminar flow preserves equipment service life while turbulent flow damages the inner surface of pipes and pumps. Based on the same hydraulic principles, our hypothesis is built on the observations that turbulent flow injures the intima and triggers atherosclerosis. In order to identify an optimal BP, at which BP level, could we evidence VISUALLY the abolishment of turbulent flow at the iliac artery as proof of correction of the injuring mechanism precipitated by HTN? Methods: 210 patients with uncontrolled HTN who underwent coronary intervention and a repeat diagnostic angiogram a few months later because of unstable angina were enrolled. At the end each coronary procedure, patients underwent iliac angiogram for deployment of closure device. In a new technique of dynamic angiography, the contrast was injected until the iliac artery was completely opacified. As the injection stopped, the blood flew down and displaced the contrast. The movements of the blood in white color above a black background could be clearly identified and analyzed. At the same time, Artificial Intelligence (Machine Learning algorithms) program had 2 models built on Python. Model 1 was based on U-net and Densenet-121 for vessel segmentation. Model 2 was used for classification and movement of flow. Model 2 was trained based on the convolutional neural network. The main measurements were the type of flow (turbulent), directions (antegrade versus retrograde) and presence of collision from slamming of the retrograde against antegrade flow. Results: At baseline, 98% patients had prolonged reversed flow with turbulence. At the 2nd iliac angiogram, if the systolic BP was &lt;110mmHg, the rate of turbulence was 10%. If the systolic BP &gt;130mmHg, the turbulence was present in 70% (p&lt;0.05) Conclusions: With the uncontrolled BP imaged as collision at the iliac artery secondary to heightened distal vascular resistance, the abolishment of turbulence and return of laminar flow confirmed that the ideal systolic BP was &lt;110mmH in the application of personalized medicine. Larger studies need to confirm the above result.